News & numbers “Unhealthy diets are a leading cause of death and disease globally, and excessive sodium intake is


one of the main culprits.” Dr Tedros Adhanom Ghebreyesus


Sleep better, live longer


Getting good sleep can play a role in supporting your overall health, according to new research presented at the American College of Cardiology’s Annual Scientific Session together with the World Congress of Cardiology. The study found that young people who have more beneficial sleep habits are incrementally less likely to die early. “We saw a clear dose-response relationship,” said Frank Qian, MD, co-author of the study. “I think these findings emphasise that just getting enough hours of sleep isn’t sufficient. You really have to have restful sleep.” The analysis involved 172,321 people with an average age of 50, 54% of whom were women. Participants were followed for a median of 4.3 years, during which time 8,681 individuals died.


Researchers assessed five different factors of quality sleep using a low-risk sleep score they created based on answers collected as part of the survey. Factors included: 1) ideal sleep duration of seven to eight hours a


night; 2) difficulty falling asleep no more than two times a week; 3) trouble staying asleep no more than two times a week; 4) not using any sleep medication; and 5) feeling well rested after waking up at least five days a week. Each factor was assigned zero or one point for each, for a maximum of five points, which indicated the highest quality sleep.


Compared to individuals who had zero to one factors, those who had all five were 30% less likely to die for any reason, 21% less likely to die from cardiovascular disease, 19% less likely to die from cancer, and 40% less likely to die of causes other than heart disease or cancer. Qian said these other deaths were likely due to accidents, infections or neurodegenerative diseases, such as dementia and Parkinson’s disease. The researchers acknowledged that data on sleep habits was self-reported and said that future research is needed to understand more about the results.


The gut and liver disease


Research from the University of Missouri School of Medicine has established a link between western diets high in fat and sugar and the development of non-alcoholic fatty liver disease, the leading cause of chronic liver disease. The research identified the western diet-induced microbial and metabolic contributors to liver disease, advancing understanding of the gut-liver axis and, in turn, the development of dietary and microbial interventions for this threat. “We’re beginning to understand how food and gut microbiota interact to produce metabolites that contribute to the development of liver disease,” said co-principal investigator, Guangfu Li. “However, the specific bacteria and metabolites, as well as the underlying mechanisms were not well understood until now. This research is unlocking the how and why.”


The gut and liver have a close anatomical and functional connection via the portal vein. Unhealthy diets change the gut


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microbiota, resulting in the production of pathogenic factors that impact the liver. By feeding mice foods high in fat and sugar, the research team discovered that the mice developed a gut bacterium called Blautia producta and a lipid that caused liver inflammation and fibrosis. That caused the mice to develop non-alcoholic steatohepatitis or fatty liver disease, with similar features to the human disease. As part of this study, the researchers also tested treating the mice with an antibiotic cocktail administered via drinking water. They found that the antibiotic treatment reduced liver inflammation and lipid accumulation, resulting in a reduction in fatty liver disease. These results suggest that antibiotic-induced changes in the gut microbiota can suppress inflammatory responses and liver fibrosis. The research team recently received a $1.2m grant from the National Institutes of Health to fund this ongoing research into the link between gut bacteria and liver disease.


DNA drugs for ALS


A study has demonstrated the effectiveness of designer DNA drugs in restoring a protein lost in patients with amyotrophic lateral sclerosis (ALS). Patients with ALS show a reduction in transactive response DNA-binding protein-43 (TDP-43), which sustains levels of the STMN2 gene responsible for encoding stathmin-2 – a protein crucial to the regeneration of neurons and the maintenance of connections to muscle fibres. Researchers from University of California San Diego School of Medicine, led by Don Cleveland, demonstrated a way to restore the production of stathmin-2 without TDP-43 in mice using designer DNA drugs. “Without stathmin-2, motor neurons disconnect from muscle, driving paralysis that is characteristic of ALS. What we have now found is that we can mimic TDP-43 function with a designer DNA drug, thereby restoring correct stathmin-2 RNA and protein level in the mammalian nervous system,” said Cleveland. “With mouse models we engineered to misprocess their stathmin-2 encoding RNAs, like in these human diseases, we show that administration of one of these designer DNA drugs into the fluid that surrounds the brain and spinal cord restores normal stathmin-2 levels throughout the nervous system.” Specifically, the researchers edited genes in mice to contain human STMN2 gene sequences and then injected antisense oligonucleotides – small bits of DNA or RNA that can bind to specific RNA molecules, blocking their ability to make a protein or changing how their final RNAs are assembled – into cerebral spinal fluid. The injections corrected STMN2 pre-mRNA misprocessing and restored stathmin-2 protein expression fully independent of TDP-43 function. “Our findings lay the foundation for a clinical trial to delay paralysis in ALS by maintaining stathmin-2 protein levels in patients using our designer DNA drug,” Cleveland said. Cleveland is broadly credited with developing the concept of designer DNA drugs, which act to either turn on or turn off genes associated with many degenerative diseases of the aging human nervous system. Several designer DNA drugs are in clinical trials for multiple diseases. One has been approved to treat a childhood neurodegenerative disease called spinal muscular atrophy.


Practical Patient Care / www.practical-patient-care.com


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